Photoprotective effect of libanoridin isolated from Corydalis heterocarpa on UVB stressed human keratinocyte cells
Photoprotective effect of libanoridin isolated from Corydalis heterocarpa on UVB stressed human keratinocyte cells
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DOI：
10.1111/exd.12085
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发表时间：
2013-02-01
影响因子：
3.6
通讯作者：
Kim, Se-Kwon
中科院分区：
文献类型：
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作者：
Ahn, Byul-Nim;Kim, Jung-Ae;Kim, Se-Kwon
紫外线B(UVB)辐射主要作用于皮肤的表皮基底细胞层，引起有害的生物效应。在本研究中，我们研究了延胡索乙素对UVB诱导的人角质形成细胞(HaCaT)损伤的保护作用及其分子机制。Libanoridin可抑制40mJ/cm2中波紫外线诱导的细胞毒性和乳酸脱氢酶。此外，Libanoridin还可降低IV型胶原酶(MMP2、MMP9)的表达水平。此外，在利巴诺里丁治疗后，增强了基质金属蛋白酶组织抑制物。此外，Libanoridin可降低UVB诱导的JNK、ERK、p38和AP-1转录因子等MAPK的磷酸化水平。我们目前的研究表明，Libanoridin具有通过ASK1-MAPK和AP-1信号通路抑制UVB诱导的细胞损伤的能力。因此，利巴诺定可以作为一种有效的天然化合物来预防UVB暴露引起的皮肤损伤。
Ultraviolet-B (UVB) irradiation acts primarily on the epidermal basal cell layer of the skin, inducing harmful biological effects. In this study, we have investigated the effect of libanoridin isolated from Corydalis heterocarpa against UVB-induced damage in human keratinocyte (HaCaT) cells and the molecular mechanism underlying those effects. Treatment with libanoridin inhibited the cell cytotoxicity and LDH induced by UVB exposure at 40mJ/cm2. Additionally, expression levels of type IV collagenases (MMP-2, MMP-9) were decreased by libanoridin. Furthermore, MMP tissue inhibitors were enhanced followed by treatment with libanoridin. Moreover, UVB-induced activation of phosphorylation of three MAPKs such as JNK, ERK, p38 and AP-1 transcription factor were decreased by treatment with libanoridin. Our present study demonstrates that libanoridin has the abilities to inhibit UVB-induced cellular damage via ASK1-MAPK and AP-1 signalling pathways. Therefore, libanoridin may be used as an effective natural compound to prevent skin damage due to UVB exposure.